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Exercise mitigates diclofenac-induced liver mitochondrial dysfunction
Estela Santos-Alves1, Ines Marques-Aleixo, Pedro Coxito
1CIAFEL - Research Centre in Physical Activity, Health and Leisure, Faculty of Sport, University of Porto, Porto, Portugal.
European Journal of Clinical Investigation
|June 4, 2014
Summary
Physical exercise, including endurance training (ET) and voluntary physical activity (VPA), protects liver mitochondria against diclofenac toxicity. Exercise enhances mitochondrial resistance to damage and modulates key proteins involved in oxidative stress and apoptosis.
Area of Science:
- Mitochondrial biology
- Exercise physiology
- Toxicology
Background:
- Non-steroidal anti-inflammatory drugs (NSAIDs) can cause liver injury.
- Strategies are needed to mitigate NSAID-induced liver damage.
- Physical exercise is explored as a protective intervention.
Purpose of the Study:
- To investigate if physical exercise protects liver mitochondria against diclofenac toxicity in vitro.
- To assess the impact of endurance training (ET) and voluntary physical activity (VPA) on mitochondrial function and integrity.
Main Methods:
- Male Sprague-Dawley rats underwent 12-week ET or VPA, alongside a sedentary group.
- In vitro liver mitochondrial function was assessed (oxygen consumption, transmembrane potential, MPTP susceptibility).
- Oxidative stress markers, apoptotic signaling, OXPHOS components, and liver morphology were analyzed.
Main Results:
- Exercise (ET and VPA) reduced susceptibility to mitochondrial permeability transition pore (MPTP) opening induced by diclofenac.
- Exercise prevented diclofenac-induced decrease in transmembrane electric potential (ΔΨ) and increased state 4 respiration.
- Exercise modulated oxidative stress markers (e.g., SIRT3, aconitase) and apoptotic regulators (e.g., Bcl-2, caspase 9).
Conclusions:
- Both ET and VPA enhanced resistance to in vitro diclofenac-induced mitochondrial dysfunction.
- Physical exercise may protect against NSAID toxicity by modulating oxidative stress and MPTP regulators.
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